British journal of pharmacology · 2026
The role of fluvoxamine in the treatment of endotoxin-induced acute heart injury.
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Ilhan Ilter, Aşcı Halil, Tepebasi Muhammet Yusuf, Hasseyid Nursel, Arlıoğlu Melih, Özmen Özlem
Аннотация
BACKGROUND AND PURPOSE: Cardiovascular diseases are among the most common health problems worldwide. Inflammation plays a critical role in the pathogenesis of various heart diseases. Lipopolysaccharides (LPS) trigger inflammatory mechanisms, leading to an inflammatory response. Fluvoxamine (FLV) is a selective serotonin reuptake inhibitor with anti-inflammatory and antioxidative properties. This study investigated the potential protective effects of FLV on sepsis-induced cardiac inflammation and injury.
EXPERIMENTAL APPROACH: Thirty-two female Wistar Albino rats were divided into four groups: control, LPS (5 mg·kg-1 intraperitoneally), LPS + FLV, and FLV (50 mg·kg-1·day-1 orally for 3 days). Thirty minutes after the final FLV administration, LPS was administered, and animals were killed 6 h later. Cardiac tissues were evaluated by histopathological analysis, immunohistochemical assessment of caspase-3, TNF-α, interleukin-1 beta (IL-1β), interleukin-6 receptor (IL-6R), IL-10, and NF-κB; biochemical determination of total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI); and gene expression analysis by real-time quantitative polymerase chain reaction (RT-qPCR) of sirtuin-1 (SIRT-1), nuclear factor erythroid 2-related factor 2 (NRF-2), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and p53.
KEY RESULTS: LPS administration significantly increased TOS, OSI, caspase-3, TNF-α, IL-1β, IL-6R, NF-κB, and p53, while decreasing IL-10, SIRT-1, NRF-2, and PGC-1α, accompanied by marked inflammatory and structural cardiac damage. FLV treatment markedly reversed these alterations, attenuating inflammation, oxidative stress, and apoptosis.
CONCLUSION AND IMPLICATIONS: These findings suggest that FLV may confer cardioprotection against LPS-induced inflammatory and apoptotic cardiac injury, potentially through modulation of IL-6R/NF-κB-mediated inflammatory signalling and the SIRT-1-NRF-2-PGC-1α axis.
EXPERIMENTAL APPROACH: Thirty-two female Wistar Albino rats were divided into four groups: control, LPS (5 mg·kg-1 intraperitoneally), LPS + FLV, and FLV (50 mg·kg-1·day-1 orally for 3 days). Thirty minutes after the final FLV administration, LPS was administered, and animals were killed 6 h later. Cardiac tissues were evaluated by histopathological analysis, immunohistochemical assessment of caspase-3, TNF-α, interleukin-1 beta (IL-1β), interleukin-6 receptor (IL-6R), IL-10, and NF-κB; biochemical determination of total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI); and gene expression analysis by real-time quantitative polymerase chain reaction (RT-qPCR) of sirtuin-1 (SIRT-1), nuclear factor erythroid 2-related factor 2 (NRF-2), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and p53.
KEY RESULTS: LPS administration significantly increased TOS, OSI, caspase-3, TNF-α, IL-1β, IL-6R, NF-κB, and p53, while decreasing IL-10, SIRT-1, NRF-2, and PGC-1α, accompanied by marked inflammatory and structural cardiac damage. FLV treatment markedly reversed these alterations, attenuating inflammation, oxidative stress, and apoptosis.
CONCLUSION AND IMPLICATIONS: These findings suggest that FLV may confer cardioprotection against LPS-induced inflammatory and apoptotic cardiac injury, potentially through modulation of IL-6R/NF-κB-mediated inflammatory signalling and the SIRT-1-NRF-2-PGC-1α axis.